In a model of Ras-driven skin cancer, Liu and colleagues showed that the RhoB-null mice had increased skin tumors compared to the heterozygote mice and that RhoB-deficient MEFs transformed with E1A and Ras showed greater resistance to DNA-damage induced apoptosis,114 which suggests that, if functional, these might be inactivating mutations. This evidence concerns the gene DHTKD1 and skin neoplasm.